The use of splice‐switching antisense therapy is promising; nevertheless, its potential to treat a variety of disorders has yet to be realized. This review discusses successes and obstacles of this approach and provides a forward look into wider application of therapeutic antisense oligonucleotides.

This is an open access article under the terms of the Creative Commons Attribution 4.0 License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

This is an open access article under the terms of the Creative Commons Attribution 4.0 License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

This is an open access article under the terms of the Creative Commons Attribution 4.0 License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

1Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Department of Immunology and Microbiology, Shanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine (SJTU‐SM), Shanghai, China

This is an open access article under the terms of the Creative Commons Attribution 4.0 License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

This is an open access article under the terms of the Creative Commons Attribution 4.0 License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Proinflammatory cytokines such as IFNγ and TNFα are known to be key mediators of cancer cachexia‐induced muscle loss. Here, they are shown to promote muscle atrophy by directly activating the transcription factor STAT3.

Synopsis

Proinflammatory cytokines such as IFNγ and TNFα are known to be key mediators of cancer cachexia‐induced muscle loss. Here, they are shown to promote muscle atrophy by directly activating the transcription factor STAT3.

This is an open access article under the terms of the Creative Commons Attribution 4.0 License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

This is an open access article under the terms of the Creative Commons Attribution 4.0 License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Numb‐deficient human breast cancer is a typical example of “cancer stem cell (CSC) disease”. Dysfunction of the Numb/p53 tumor suppressor circuitry in these tumors results in expansion of CSCs with altered self‐renewing divisions and high tumorigenic potential.

Synopsis

Numb‐deficient human breast cancer is a typical example of “cancer stem cell (CSC) disease”. Dysfunction of the Numb/p53 tumor suppressor circuitry in these tumors results in expansion of CSCs with altered self‐renewing divisions and high tumorigenic potential.

This is an open access article under the terms of the Creative Commons Attribution 4.0 License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

1Laboratory for Molecular Respiratory Carcinogenesis, Department of Physiology, Faculty of Medicine, University of Patras, Rio, Greece

2Comprehensive Pneumology Center (CPC) and Institute for Lung Biology and Disease (iLBD), Member of the German Center for Lung Research (DZL), University Hospital, Ludwig‐Maximilians University and Helmholtz Center Munich, Munich, Germany

3Pneumology Unit, Department of Pediatrics, Faculty of Medicine, University of Patras, Rio, Greece

4Department of Radiation Oncology and Stereotactic Radiotherapy, Faculty of Medicine, University of Patras, Rio, Greece

Mutations in the NRAS oncogene are shown to promote lung metastasis by regulating chemokine expression in tumor cells and hence their affinity for the pulmonary vasculature and their ability to form metastatic niches.

Synopsis

Mutations in the NRAS oncogene are shown to promote lung metastasis by regulating chemokine expression in tumor cells and hence their affinity for the pulmonary vasculature and their ability to form metastatic niches.

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The pathogenic G4C2 repeat expansion upstream of C9orf72 is bidirectionally transcribed and translated into five aggregating dipeptide repeat proteins (DPRs). Analysis of cell‐to‐cell transmission of DPRs suggests that DPR‐directed antibodies may have therapeutic potential.

Synopsis

The pathogenic G4C2 repeat expansion upstream of C9orf72 is bidirectionally transcribed and translated into five aggregating dipeptide repeat proteins (DPRs). Analysis of cell‐to‐cell transmission of DPRs suggests that DPR‐directed antibodies may have therapeutic potential.

The hydrophobic DPR species poly‐GA, poly‐GP and poly‐PA are transmitted between cells.

This is an open access article under the terms of the Creative Commons Attribution 4.0 License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

This is an open access article under the terms of the Creative Commons Attribution 4.0 License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Both overexpression and seeding of wild‐type α‐synuclein in mice affects cortical dendritic spine density and dynamics and impairs structural plasticity in an age‐dependent manner. These data provide insights into the pathophysiology underlying dementia associated with α‐synucleinopathies.

Synopsis

Both overexpression and seeding of wild‐type α‐synuclein in mice affects cortical dendritic spine density and dynamics and impairs structural plasticity in an age‐dependent manner. These data provide insights into the pathophysiology underlying dementia associated with α‐synucleinopathies.

In vivo dynamics of dendritic spine formation is reduced in young adult PDGF‐h‐α‐syn mouse brains.

In older mice, overall spine loss is compensated by an increase in spine turnover in vivo.

Plastic changes are reflected by changes in spine morphology.

Seeding of preformed α‐synuclein fibrils causes similar alterations in dendritic spine density and morphology as well as dendritic swellings.

This is an open access article under the terms of the Creative Commons Attribution 4.0 License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.